CERT1 Knockout HeLa Cell Line
Cat.No.:
EDC08305
Species:
Human
Cell Name:
HeLa
Gene:
CERT1
Gene ID:
10087
Size:
1×10⁶cells
CERT1 Knockout Cell Line (Hela) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
| Cat.No. | EDC08305 |
|---|---|
| Product Name | CERT1 Knockout Hela Cell Line |
| Cell Line | Hela |
| Cellosaurus ID | CVCL_0030 |
| Cell Line Synonyms | HELA, Hela, He La, He-La, HeLa-CCL2, Henrietta Lacks cells, Helacyton gartleri |
| Gene | CERT1 |
| NCBI Gene ID | |
| Gene Synonyms | CERT|CERTL|COL4A3BP|GPBP|MRD34|NEDHSF|STARD11 |
| Summary |
This gene encodes a kinase that specifically phosphorylates the N-terminal region of the non-collagenous domain of the alpha 3 chain of type IV collagen, known as the Goodpasture antigen. Goodpasture disease is the result of an autoimmune response directed at this antigen. One isoform of this protein is also involved in ceramide intracellular transport. Three transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
|
| Associated Diseases | Cervical Carcinoma |
| Morphology | Adherent |
| Passage Ratio | 1/5, 2days |
| Complete Culture Medium | MEM + 10% FBS |
| Freezing Medium | 70%Complete culture medium+ 20% FBS+ 10% DMSO |
| QC | Indels validated by Sanger sequencing; sterility confirmed via microbial testing. |
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
| Loci | STR Info (Sample Cell) Sample Cell Line: HeLa | STR Info (Cell bank) Cell Line: HeLa | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | X | ||
| CSF1PO | 9 | 10 | 9 | 10 |
| D1S1656 | 12 | 15 | 12 | 15 |
| D2S1338 | 17 | 17 | ||
| D3S1358 | 15 | 18 | 15 | 18 |
| D5S818 | 11 | 12 | 11 | 12 |
| D6S1043 | 18 | 18 | ||
| D7S820 | 8 | 12 | 8 | 12 |
| D8S1179 | 12 | 13 | 12 | 13 |
| D12S391 | 20 | 25 | 20 | 25 |
| D13S317 | 12 | 14 | 12 | 14 |
| D16S539 | 9 | 10 | 9 | 10 |
| D18S51 | 16 | 16 | ||
| D19S433 | 13 | 14 | 13 | 14 |
| D21S11 | 27 | 28 | 27 | 28 |
| FGA | 18 | 21 | 18 | 21 |
| Penta D | 8 | 15 | 8 | 15 |
| Penta E | 7 | 17 | 7 | 17 |
| TPOX | 8 | 12 | 8 | 12 |
| VWA | 16 | 18 | 16 | 18 |
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.
Conclusion: The STR identification of this cell is correct.
FAQ
Which is better for studying CERT1 function, CERT1 Knockout HeLa Cell Line or CERT1 overexpression HeLa Cell Line?
The choice depends on whether you are studying CERT1 (ceramide transfer protein 1, COL4A3BP, STARD11)'s role as a non-vesicular ceramide transporter or modeling its functions in sphingolipid biology and emerging neurodevelopmental disease. The Knockout line is the standard tool for asking whether CERT1 is required for these processes — CERT1 is a START-domain containing protein that mediates non-vesicular transfer of ceramide from the ER to the trans-Golgi network for sphingomyelin and glucosylceramide synthesis; CERT1 has N-terminal PH domain (Golgi PI4P binding), middle FFAT motif (ER VAP binding), and C-terminal START domain (ceramide binding). Overexpression is useful for studying CERT1 in heterologous expression contexts.
For sphingolipid biology research, the EDITGENE CERT1 Knockout in HeLa is highly informative — CERT1 de novo heterozygous mutations cause autosomal dominant intellectual disability syndrome (NEDMIAH, neurodevelopmental disorder with intellectual disability and seizures). Rescue with wild-type, ceramide-binding-deficient (G67E START domain), or NEDMIAH-associated CERT1 mutations enables comprehensive structure-function and disease modeling. The knockout is valuable for studying ER-Golgi non-vesicular lipid transfer and CERT1-related neurodevelopmental disorder mechanisms.
What are the application scenarios for this model?
Primary applications:
• Non-vesicular ceramide transfer: ER-to-Golgi ceramide transport analysis in CERT1-null cells.
• Sphingolipid metabolism: sphingomyelin and glucosylceramide synthesis analysis given CERT1-dependent ceramide supply to TGN.
• NEDMIAH modeling: rescue with de novo heterozygous CERT1 mutations causing intellectual disability syndrome.
• ER-Golgi contact sites: ER-TGN membrane contact site analysis given CERT1's FFAT motif-PH domain bridge function.
EDITGENE recommends this model for researchers investigating non-vesicular lipid transfer, sphingolipid biology, and CERT1-related neurodevelopmental disorder.
Is this CERT1 Knockout HeLa Cell Line compatible with overexpression rescue experiments?
Yes. CERT1 rescue experiments are well-established for non-vesicular lipid transfer research:
• Construct design: use a codon-modified CERT1 sequence with a small C-terminal tag (FLAG, HA). CERT1 has N-terminal PH domain (Golgi PI4P binding), middle FFAT motif (ER VAP-A/B binding), and C-terminal START domain (ceramide binding) — preserve all elements.
• Ceramide-binding-deficient rescue: G67E mutation in the START domain abolishes ceramide binding.
• PH-deficient rescue: PH domain mutations disrupt Golgi PI4P binding.
• FFAT-mutant rescue: FFAT motif mutations disrupt ER VAP binding.
• NEDMIAH mutation rescue: de novo heterozygous CERT1 mutations enable disease modeling.
• Functional readout: rescue should restore ER-Golgi ceramide transfer and sphingomyelin synthesis.
HeLa transduces efficiently with lentivirus and supports stable rescue line generation.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.